Year: 2024
Type: editorial
Abstract: Reticulophagy selectively degrades fragments of the endoplasmic reticulum (ER) through macroautophagy/autophagy to maintain ER homeostasis. The deficiency of reticulophagy results in the unfolded protein response (UPR), which is a crucial clue to the pathogenesis of inflammatory diseases. However, the detailed mechanism underlying the cross-regulation between reticulophagy and inflammatory diseases remains largely unclear. Recently, we have revealed that UBAC2 (UBA domain containing 2) is essential for controlling ER homeostasis as a novel reticulophagy receptor. MARK2 catalyzes the phosphorylation of UBAC2 at serine (S) 223, hence facilitating the progression of reticulophagy and inhibiting ER stress-induced inflammatory responses.
Source: Autophagy
Authors: Xing He, Shouheng Jin
Institution: Sun Yat-sen University
Language: English
Subfield: Epidemiology
Field: Medicine
Domain: Health Sciences
Open Access status: green
Funders: National Natural Science Foundation of China, Sun Yat-sen University, Natural Science Foundation of Guangdong Province, National Key Research and Development Program of China, Fundamental Research Funds for the Central Universities, Basic and Applied Basic Research Foundation of Guangdong Province
OpenAlex ID: W4404648651